Reference Database

Characterization of the autoimmune response against the nerve tissue S100β in patients with type 1 diabetes.
Gómez-Touriño, I
Simón-Vázquez, R
Alonso-Lorenzo, J
Arif, S
Calviño-Sampedro, C
González-Fernández, Á
Pena-González, E
Rodríguez, J
Viñuela-Roldán, J
Verdaguer, J
Cordero, O J
Peakman, M
Varela-Calvino, R
Clinical and experimental immunology 2015 May;180: 207-17

Type 1 diabetes results from destruction of insulin-producing beta cells in pancreatic islets and is characterized by islet cell autoimmunity. Autoreactivity against non-beta cell-specific antigens has also been reported, including targeting of the calcium-binding protein S100β. In preclinical models, reactivity of this type is a key component of the early development of insulitis. To examine the nature of this response in type 1 diabetes, we identified naturally processed and presented peptide epitopes derived from S100β, determined their affinity for the human leucocyte antigen (HLA)-DRB1*04:01 molecule and studied T cell responses in patients, together with healthy donors. We found that S100β reactivity, characterized by interferon (IFN)-γ secretion, is a characteristic of type 1 diabetes of varying duration. Our results confirm S100β as a target of the cellular autoimmune response in type 1 diabetes with the identification of new peptide epitopes targeted during the development of the disease, and support the preclinical findings that autoreactivity against non-beta cell-specific autoantigens may have a role in type 1 diabetes pathogenesis.

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